Repair and pain · part of Injury, healing and recovery and Immune system and inflammation and Gut health
Does it bring inflammation down?
Almost always measured as a marker in blood rather than as something a person notices. Worth knowing which one a trial actually moved.
59,291
people in trials
12
studies in people
15
compounds, animal or lab only
1
compounds people report on
3
trials found nothing
Measured in people
A trial that gave people the compound comes first. A study that only watched people, who happened to have more or less of something related, comes after. Both are studies in people and both are here. Only the first kind tested the thing you are asking about, and the watch-only ones are labelled. Within that, the most people come first. That is a fact about the studies, not a judgement about the compound. Counts are never added up across compounds, because the same person can be in more than one trial.
Peptides and blends
3 compounds · 62 people given one of themWhat this archive is for. Trials of the compound come first, ranked by how many people were actually given it. Studies that only observed people are below them and labelled.
- 01ThymalinPeptideModerate. At least one finished study in people, and at least 100 people who took it. 4 completed trials, 308 people given it.7 reported42 people given it1 trial
A small early-pandemic trial reported faster recovery, and nobody died in either group. 42 patients got thymalin injections into the muscle for five days on top of standard care, and 50 got standard care alone, at one hospital in mid 2020. Lung scans worsened in 2 of the 42 treated against 5 of the 50 controls. Markers of inflammation fell faster on the drug. Everybody knew who was getting it. With no deaths at all, the trial cannot say whether thymalin saves lives.
The numbers Single-centre, open-label, prospective randomized controlled trial, April to July 2020: 42 patients received thymalin 10 mg intramuscularly daily for 5 days plus standard care, 50 received standard care. No deaths in either group. Radiological progression in 2 of 42 treated against 5 of 50 controls, with faster falls in IL-6, C-reactive protein and D-dimer.
Stem Cell Reviews and Reports, 2021· 42 people
- 02BrimapitidePeptideModerate. At least one finished study in people, and at least 100 people who took it. 4 completed trials, 510 people given it.20 people given it1 trial
A small safety study in inflamed eyes, with nothing to compare it against. Twenty people who had inflammation inside the eye after surgery or injury got one injection under the surface of the eye. Seventeen side effects were recorded and all were judged unrelated to the drug. Almost none of the peptide reached the bloodstream. Inflammation did fall. Everybody got the drug, so there is no way to know whether it would have settled anyway. The paper does not say who paid.
The numbers Phase 1b, 20 patients with post-surgical or post-traumatic intraocular inflammation, single subconjunctival dose of 45, 90, 450 or 900 mcg (5 per group). 17 non-serious adverse events judged unrelated to treatment; plasma peptide undetectable in the three lower dose groups. No control group, so the observed fall in inflammation cannot be attributed to the drug. Funding not stated in the abstract.
Journal of Ocular Pharmacology and Therapeutics, 2015· 20 people
- 03BPC-157PeptideLimited. People have taken it in a published study, but fewer than 100 of them. 3 completed trials, 31 people given it.10 reported0 people given it1 trial
A company registered a study of a BPC-157 gummy, marked it completed, and has posted no results. 40 physically active adults were to take two gummies a day for eight weeks, 500 mcg of BPC-157 per serving. The main measurements were two blood markers of inflammation, hs-CRP and IL-6. Everybody was to get the gummy. There was no dummy gummy to compare against.
The numbers Single-arm 8-week study of a 500 mcg BPC-157 gummy in 40 physically active adults, primary endpoints hs-CRP and IL-6. Listed as completed in November 2025 with no results posted.
ClinicalTrials.gov, Parlay Wellness, 2025· number of people not given
Supplements
2 compounds · 245 people given one of themVitamins, minerals, amino acids and botanicals sold over the counter, held to the same standard.
- 01ResveratrolSupplementModerate. At least one finished study in people, and at least 100 people who took it. 14 completed trials, 403 people given it.7 reported203 people given it2 trials1 found nothing
found nothingThe longest and largest diabetes trial of resveratrol found nothing that counted. 192 patients took 40 mg, 500 mg or a dummy pill every day for six months. An inflammation marker fell further on resveratrol, but not by enough to call real. Weight, waist, blood pressure, blood sugar, insulin and a string of other markers did not change. Cholesterol and triglycerides rose slightly on the high dose. Patients earlier in their diabetes did show a real fall in inflammation.
The numbers The largest and longest diabetes trial here: 192 patients, 40 or 500 mg per day for six months. CRP fell 5.6% and 15.9% versus placebo but not significantly, and there was no significant change in weight, BMI, waist, blood pressure, fasting glucose, HbA1c, insulin, C-peptide, free fatty acids, liver enzymes, uric acid, adiponectin or IL-6. Total cholesterol and triglycerides rose slightly on 500 mg. Subgroups with shorter diabetes duration did show a significant CRP reduction.
Pharmacological Research, 2016· 192 people
This is the strongest good human result resveratrol has, and it rests on eleven men. Obese but otherwise healthy men took 150 mg a day for a month, and also spent a month on a dummy pill. Their resting metabolism slowed the way it does when people eat less. Liver fat, blood sugar, triglycerides, a liver enzyme and inflammation markers all fell. Blood pressure improved. Muscle samples showed the cell's energy machinery switched on.
The numbers Eleven healthy obese men, randomised double-blind crossover, 150 mg per day for 30 days. Sleeping and resting metabolic rate fell; muscle AMPK was activated with higher SIRT1 and PGC-1alpha protein and improved mitochondrial respiration on a fatty-acid substrate; intrahepatic lipid, circulating glucose, triglycerides, ALT and inflammation markers fell; systolic blood pressure and HOMA improved. The strongest positive mechanistic human result in the literature, in eleven men.
Cell Metabolism, 2011· 11 people
What people using it report
- Interest leans toward blood test numbers people cannot feel. Posters more often talk about checking cholesterol, blood sugar or CRP than about any change in energy, mood or thinking they noticed day to day.
- 02MIB-626SupplementModerate. At least one finished study in people, and at least 100 people who took it. 4 completed trials, 107 people given it.1 reported42 people given it1 trial1 found nothing
found nothingThe tablet raised NAD in very sick patients and made no difference to them. 42 adults in hospital with COVID-19 and sudden kidney injury took MIB-626 or dummy tablets twice a day for two weeks. NAD in the blood roughly doubled by the end. Kidney blood tests came out the same in both groups. So did inflammation markers and how ill people were. The authors want the drug tried as a drip instead. Two authors work for the manufacturer and a third consults for it.
The numbers NCT05038488. 42 adults hospitalised with COVID-19 and acute kidney injury randomised 3:2 to MIB-626 1.0 g or placebo tablets twice daily for 14 days. Blood NAD rose gradually from 16.0 to 25.5 to 42.6 micrograms per millilitre at baseline, day 5 and day 14, and NAD metabolites rose rapidly by day 3. Serum creatinine, cystatin C and serum markers of acute kidney injury did not differ between groups. Serum CRP, IL-6 and TNF alpha and indices of disease severity also did not differ. The authors attribute the absence of clinical effect to the slow rise in NAD and call for studies of parenteral administration. Two authors are employees of Metro International Biotech and a third is a consultant to the company.
FASEB BioAdvances, 2025· 42 people
Other compounds
4 compounds · 5,082 people given one of themApproved drugs, biologics and hormones that have been measured for this. They are here because leaving them out would misrepresent the evidence, and they are below the peptides because that is not what most people come here to read.
- 01MethotrexateSmall moleculeStrong. At least two finished studies in people, and at least 1,000 people who took it. 2 completed trials, 5,022 people given it.4 reported5,022 people given it2 trials1 found nothing
found nothingLow-dose methotrexate did not prevent heart attacks or strokes in people who already had heart disease, and it did not lower the inflammation markers it was supposed to. 4,786 people took it or a dummy pill for about two years, and all took folate too. This is the trial that separates methotrexate from the inflammation story it was borrowed for. It was stopped early. It carried real side effects, including liver enzyme rises, lower blood counts and more skin cancers.
The numbers 4,786 patients with previous myocardial infarction or multivessel coronary disease plus type 2 diabetes or metabolic syndrome, randomised double-blind to methotrexate 15 to 20 mg weekly or placebo, all on 1 mg folate daily, median follow-up 2.3 years, stopped early. Methotrexate did not reduce cardiovascular events: primary endpoint in 201 versus 207 patients (4.13 versus 4.31 per 100 person-years, HR 0.96, 95% CI 0.79 to 1.16), and it did not reduce IL-1 beta, IL-6 or CRP. More liver enzyme elevations, lower leukocyte counts and haematocrit, and more non-basal-cell skin cancers on methotrexate.
The New England Journal of Medicine, 2019· 4,786 people
A year of methotrexate given before rheumatoid arthritis was diagnosed did not stop the arthritis from arriving. 236 adults with joint pain took part. They also got one steroid shot at the start. They did have less pain, stiffness and joint inflammation two years on. One region, and an early test of the idea.
The numbers 236 adults with arthralgia and MRI-detected subclinical joint inflammation randomised double-blind to a single 120 mg intramuscular glucocorticoid injection plus 1 year of oral methotrexate up to 25 mg weekly, or placebo, followed for 2 years. Persistent clinical arthritis in 19% versus 18% (HR 0.81, 95% CI 0.45 to 1.48). Physical functioning (HAQ difference -0.09), pain (-8 on a 0 to 100 scale), morning stiffness (-12) and MRI-detected inflammation (-1.4 points) better on methotrexate; serious adverse events equal.
The Lancet, 2022· 236 people
- 02SomatropinBiologicLimited. People have taken it in a published study, but fewer than 100 of them. 2 completed trials, 84 people given it.9 reported60 people given it1 trial
Take growth hormone away from adults who need it and most things get worse. 60 adults with a pituitary shortage, treated for about ten years, were switched onto a dummy for four months. Their IGF-1 fell sharply. Two aspects of quality of life declined. Waists grew, deep belly fat rose, and cholesterol and an inflammation marker worsened. One thing improved: their response to insulin got better. This is about people with a diagnosed shortage, not about anybody whose own levels are normal.
The numbers 60 hypopituitary adults on GH for a mean of 10 years were crossed over to four months of placebo. IGF-1 fell from 168 to 98 micrograms per litre, two quality-of-life domains deteriorated, waist circumference and visceral fat rose, and lipids and C-reactive protein worsened, while insulin sensitivity improved.
Journal of Clinical Endocrinology and Metabolism, 2012· 60 peoplepoints the wrong way
- 03Metformin plus rapamycinSmall moleculePreliminary. Studied in people, but no published study has had people take it. 2 registered with no result.2 reported0 people given it1 trial
The one trial testing this pair cannot tell the two drugs apart. 30 people are enrolled by AgelessRx, an online company that prescribes these drugs, and it is no longer signing people up. Every group stacks rapamycin and metformin together with low-dose naltrexone, NAD+ up the nose, glutathione on the skin and a house-brand supplement. With six things given at once, no result could be traced to either drug. Nothing has been posted.
The numbers 30 participants, sponsor AgelessRx (a telehealth prescriber), active not recruiting. Arms combine rapamycin 2 to 6 mg weekly, metformin 500 mg daily, low-dose naltrexone, intranasal NAD+, topical glutathione and a proprietary supplement; primary endpoints VO2 max, a cognitive composite and an inflammation index. Cannot isolate either drug. No results posted.
ClinicalTrials.gov, 2025· number of people not given
- 04GDF15BiologicModerate. At least one finished study in people, and at least 100 people who took it. 2 completed trials, 313 people given it.3 reportednobody was given it2 watch-only studies
GDF15 tracks with getting sick in general, not with any one disease. Researchers measured thousands of blood proteins in 53,026 UK adults and followed them for over 13 years. Higher GDF15 went with later diagnosis of more than twenty different long-term illnesses, and with having several at once. Much of the level was explained by kidney function, liver function, inflammation and body fat. Nobody was given anything here. This is a marker of trouble, not a proven cause of it.
The numbers UK Biobank proteomics, 53,026 participants, 13.3 years of follow-up: GDF15 was positively associated with 20 to 24 incident chronic diseases (hazard ratios 1.21 to 3.77) and with multimorbidity, with levels largely explained by renal function, liver function, inflammation and obesity.
Metabolism, 2025· 53,026 peopleobserved only, nobody was given it
Higher GDF15 marked out men who died sooner, but nobody was given anything. 876 Swedish men aged 35 to 80 gave a blood sample and were then followed for up to 14 years. Those with more GDF15 at the start were roughly three times as likely to die of any cause. The pattern held in a separate set of 324 twins. This is a group watched over time, not a trial. It cannot tell you whether lowering GDF15 would help anyone.
The numbers 876 Swedish men aged 35 to 80 followed up to 14 years: serum GDF15 at entry predicted all-cause mortality with an adjusted odds ratio of 3.38 (95 percent CI 1.38 to 8.26), validated in 324 same-sex twins and independent of telomere length, IL-6 and CRP. An association in a cohort, not an intervention.
Aging Cell, 2010· 876 peopleobserved only, nobody was given it
What people using these actually report
These are people describing their own use. They come from clinic write-ups, complaint records kept by regulators, and public forums, and they are shown as written. They are the best guide on this page to what people actually do, what they expect, and what goes wrong. They cannot show that anything works. Nobody was compared with people on a dummy pill, and people who saw no effect mostly stopped posting. Both things are true at once. The bad reports are kept in for the same reason.
- Interest leans toward blood test numbers people cannot feel. Posters more often talk about checking cholesterol, blood sugar or CRP than about any change in energy, mood or thinking they noticed day to day.
Sources: LONGECITY's Resveratrol subforum (including a long-running 'Positive, Negative, ZERO, effect noticed?' poll thread and a dedicated side-effects thread), general web search of longevity-community and vendor commentary on dosing, form and piperine practice, and Peter Attia's public podcast and written statements. Direct access to r/longevity, r/Supplements and r/Biohackers on Reddit was not available in this research pass (Reddit pages could not be fetched and did not surface in general web search here), so those specific subreddits could not be independently checked and any overlap with the sentiment described above is inferred, not confirmed firsthand.
Measured in animals or in the lab, not yet in people
These are kept apart from the studies in people, not ranked against them. They answer a different question. A result in a rat is a real result, and a reason somebody ran the study. It is not a measure of what happens in you. When the work in people is missing, the reason is usually money, not failure. The bottom of this page explains why.
Peptides and blends
- 01KPVPeptideAnimal or lab only. Only animal or lab studies on this page. No study in people yet. 2 animal studies, no human study.6 reported1 animal or lab study
Measured in animals or in the lab
In mice with colitis, KPV carried in tiny particles sped up healing of the gut lining and lowered a swelling signal called TNF-alpha.
The numbers Nanoparticle-delivered KPV accelerated mucosal healing and lowered TNF-alpha in a mouse colitis model.
Molecular Therapy, 2017· animal study
- 02ThymulinPeptideAnimal or lab only. Only animal or lab studies on this page. No study in people yet. 1 animal study, no human study.1 reported1 animal or lab study
Measured in animals or in the lab
In rats. A thymulin copy called PAT cut pain and swelling caused by a bacterial toxin, more so at higher doses.
The numbers A thymulin analogue (PAT) dose-dependently reduced endotoxin-induced hyperalgesia and inflammation in rats.
British Journal of Pharmacology, 2002· animal study
- 03KLOW blendBlendLimited. People have taken it in a published study, but fewer than 100 of them. 1 completed trial, 13 people given it.11 reported1 animal or lab study
Measured in animals or in the lab
In mice with gut inflammation. KPV given alone led to faster recovery, more weight regained and less inflammation in the colon. Nothing here tests KPV in a mix or in people.
The numbers In two mouse colitis models KPV led to earlier recovery, greater body-weight regain, fewer inflammatory infiltrates and lower myeloperoxidase activity in colon tissue. Mouse gut inflammation with KPV given alone; nothing here tests KPV in a blend or in people.
Inflammatory Bowel Diseases, 2008· animal study
- 04ChonlutenPeptideAnimal or lab only. Only animal or lab studies on this page. No study in people yet. 2 lab studies, no human study.2 reported1 animal or lab study
Measured in animals or in the lab
In a dish. In human immune cells, it cut the release of an inflammation signal after the cells met a bacterial toxin. The study was run with the institute that makes it, so it is not independent.
The numbers In THP-1 human monocytes, the Chonluten tripeptide cut TNF release from LPS-stimulated cells and, with the four other Khavinson peptides tested, reduced TNF and IL-6 expression and adhesion to activated endothelium. Cell culture only; the study was run with the Khavinson institute, so it is not independent of the originating research lineage.
International Journal of Molecular Sciences, 2022· lab (cells in a dish)
- 05Ac-SDKPPeptideAnimal or lab only. Only animal or lab studies on this page. No study in people yet. 1 animal study, no human study.2 reported1 animal or lab study
Measured in animals or in the lab
In rats. It cut inflammation after brain injury.
The numbers Reduced inflammation after injury in rats.
Journal of Neurosurgery, 2017· animal study
- 06RisuteganibPeptideModerate. At least one finished study in people, and at least 100 people who took it. 2 completed trials, 263 people given it.1 animal or lab study
Measured in animals or in the lab
In a dish. Retina support cells were made with mitochondria from 5 people with AMD and 3 without. They were treated with each drug for 48 hours at doses like those used in the eye. The AMD cells showed more signs of cell death at the start. The two drugs changed cell death, stress and swelling genes in different ways. This is cell work only. Public and charity money paid.
The numbers Retinal pigment epithelial cybrid cell lines carrying mitochondria from 5 AMD and 3 normal donors treated with clinical dose equivalents of each drug for 48 hours. AMD cybrids had higher baseline caspase activity; the two drugs produced different patterns of apoptosis, oxidative stress and inflammation gene expression. Cell work only. NIH and foundation funded.
Experimental Eye Research, 2021· lab (cells in a dish)
- 07CartalaxPeptideAnimal or lab only. Only animal or lab studies on this page. No study in people yet. 4 lab studies, no human study.8 reported1 animal or lab study
Measured in animals or in the lab
In a dish. Aging cartilage cells gave off more aging and inflammation signals. Both Cartalax and a cartilage extract pushed those signals back toward normal. These were cells, not joints, and nobody measured a real health result.
The numbers Cell culture. The senescence-associated secretory phenotype of chondrocytes was characterised by raised p16, p21 and p53, raised TNF-alpha and IL-1-alpha, and lowered Sirt1. Both the AED peptide and a cartilage polypeptide complex normalised the synthesis of those molecules. Chondrocytes in culture, not joints, and no clinical endpoint was measured.
Advances in Gerontology, 2023· lab (cells in a dish)
- 08ApelinPeptideLimited. People have taken it in a published study, but fewer than 100 of them. 3 completed trials, 68 people given it.3 reported1 animal or lab study
Measured in animals or in the lab
Mostly in mice. Mice missing apelin or its receptor lost a lot of muscle with age. Giving apelin signals back improved their muscle. A human part only watched people. In older people, muscle made less apelin with age, and more apelin went with more benefit from exercise. Nobody was given apelin. Public money paid for the work.
The numbers Apelin production by contracting muscle falls with age in humans and rodents and associates with exercise benefit in older people (observational). Mice lacking apelin or its receptor showed marked age-related muscle deterioration, and restoring apelin signalling improved muscle function via mitochondrial biogenesis, autophagy, anti-inflammatory pathways and muscle stem cells. The interventions are all in mice; PubMed's phase 3 trial label refers to the embedded human cohort, not to apelin administration. Non-US government funded.
Nature Medicine, 2018· animal studypoints the wrong way
Other compounds
- 01OSK Partial ReprogrammingBiologicPreliminary. Studied in people, but no published study has had people take it. 1 registered with no result.5 reported1 animal or lab study
Measured in animals or in the lab
In normally ageing mice, not ones bred to age fast, long stretches of partial reprogramming changed the kidney and skin. The longer the treatment ran, the bigger the change. Ageing clocks read younger. Genes for inflammation, worn-out cells and stress were turned down. The authors did not claim these mice lived longer.
The numbers Mouse, physiologically ageing wild-type rather than progeroid. Long-term partial reprogramming regimens produced duration-dependent effects in kidney and skin, with reversion of epigenetic clock measures and reduced inflammation, senescence and stress-response gene expression. The authors make no lifespan extension claim for wild-type mice.
Nature Aging, 2022· animal study
- 02E5 Plasma FractionProcedureAnimal or lab only. Only animal or lab studies on this page. No study in people yet. 4 animal studies, no human study.4 reported1 animal or lab study
Measured in animals or in the lab
In rats, a fraction of young pig plasma made old organs look much younger on paper. The team first built and checked six tissue-age clocks for rat tissue, from 613 samples. Two of those also work in human tissue. After treatment, the tissue age of blood, heart and liver more than halved. A control centre in the brain moved less but still moved. Blood tests, body function, behaviour and memory all improved. Funded by the US National Institutes of Health with other support.
The numbers Rat. Six epigenetic clocks were developed and validated for rat tissues from 613 tissue samples, with two clocks trained on an additional 1,366 human tissue samples to work across both species. A young porcine plasma fraction treatment more than halved the epigenetic ages of blood, heart and liver tissue in old rats, with a smaller but statistically significant effect in hypothalamus, accompanied by improvements in biochemical, physiological, behavioural and cognitive measures and a shift in immunoglobulin G N-glycosylation from pro- to anti-inflammatory. NIH supported with non-US government funding.
GeroScience, 2024· animal study
- 03ClusterinBiologicPreliminary. Studied in people, but no published study has had people take it. 2 human studies where nobody was given it, 1 registered with no result.4 reported1 animal or lab study
Measured in animals or in the lab
In mice, with one human measurement inside it. Plasma from mice that chose to run, given to mice that did not, quietened inflammation genes in the brain. Protein screening showed a rise in a set of immune system brakes, clusterin among them. Clusterin injected into a vein stuck to the lining of brain blood vessels and quietened those genes, in two different models. Separately, people with memory problems who did six months of structured exercise had more clusterin in their blood.
The numbers Mouse, with a human observational component. Plasma from voluntarily running mice infused into sedentary mice reduced baseline neuroinflammatory gene expression and experimentally induced brain inflammation. Proteomics showed a coordinated increase in complement cascade inhibitors including clusterin. Intravenous clusterin bound brain endothelial cells and reduced neuroinflammatory gene expression in acute brain inflammation and Alzheimer models. Separately, patients with cognitive impairment who completed six months of structured exercise had higher plasma clusterin. NIH funded.
Nature, 2021· animal study
- 0425-HydroxycholesterolSmall moleculePreliminary. Studied in people, but no published study has had people take it. 1 human study where nobody was given it.2 reported1 animal or lab study
Measured in animals or in the lab
In mice. In mice with clogged arteries, 25-hydroxycholesterol made by immune cells made artery swelling and damage worse. It was also measured in human artery tissue, but only measured. This is a harm result in the same part of the body as the artery stiffness study.
The numbers Mouse atherosclerosis models, with 25-hydroxycholesterol and CH25H expression also measured in human lesions. Macrophage-derived 25-hydroxycholesterol promoted vascular inflammation and lesion remodelling, a harm direction in the same organ system as the aortic stiffness study.
Circulation, 2023· animal studypoints the wrong way
- 0517-alpha-estradiolHormoneAnimal or lab only. Only animal or lab studies on this page. No study in people yet. 4 animal studies, no human study.4 reported1 animal or lab study
Measured in animals or in the lab
In mice, this study asked why these drugs mostly help males. It found that the drop in brain inflammation was itself different between males and females. That is part of an answer, not the whole answer.
The numbers A mechanistic follow-up asking why these effects are sex-specific, reporting that the reduction in hypothalamic inflammation itself differs by sex. A partial answer rather than a resolution.
Aging Cell, 2017· animal study
- 06LamivudineSmall moleculeLimited. People have taken it in a published study, but fewer than 100 of them. 1 completed trial, none stating how many people.3 reported1 animal or lab study
Measured in animals or in the lab
In mice and in a dish. This is the paper that started the idea. In worn-out cells, jumping genes woke up and set off an immune alarm through loose DNA copies. Drugs that block the copying stopped it. Giving lamivudine to old mice turned down the alarm and cut inflammation in several body parts. It measured inflammation, not lifespan. The paper has a published author correction, which is not a retraction.
The numbers The founding paper. LINE-1 elements become transcriptionally derepressed during cellular senescence and activate a type I interferon response, triggered by cytoplasmic LINE-1 complementary DNA and blocked by LINE-1 reverse transcriptase inhibitors. Treating aged mice with lamivudine downregulated interferon activation and age-associated inflammation in several tissues. Inflammation endpoints, not survival. The paper carries a published author correction in Nature in 2019, which is a correction and not a retraction.
Nature, 2019· animal study
- 07RuxolitinibSmall moleculeModerate. At least one finished study in people, and at least 100 people who took it. 1 completed trial, 309 people given it.1 animal or lab study
Measured in animals or in the lab
In human cells in a dish and in old mice. Blocking the JAK pathway quieted the inflammatory signals from zombie cells. In old mice, 10 weeks of a JAK-blocking drug cut inflammation and helped them move better. There is no result in people.
The numbers Human cells in culture plus aged mice. Senescent human preadipocytes and HUVECs developed a SASP that was suppressed by JAK-pathway RNAi or JAK inhibitors, and conditioned medium from JAK-inhibitor-treated senescent cells was much less proinflammatory. Giving a JAK inhibitor to aged mice for 10 weeks alleviated adipose and systemic inflammation and enhanced physical function. The authors state their findings are consistent with a possible contribution of senescent cells to age-related frailty and speculate about SASP inhibition; they do not report a human outcome.
Proceedings of the National Academy of Sciences, 2015· animal study
Why the trial record looks like this
A missing trial usually means nobody would pay for it. Nobody spends hundreds of millions of dollars on a molecule they cannot own. So the compounds with the thinnest record in people are often the oldest and easiest to get, not the weakest. Taking KPV as the example, because it states the problem most clearly:
KPV is three amino acids, lysine, proline and valine, taken from the tail of a human hormone. It is about as impossible to own as a molecule gets, and the record shows what that produces. A few university labs have found it interesting in mice for nearly twenty years, and no company has ever tested it in a person.
The same hormone family shows what money buys when there is money. Where a new version could be patented, companies paid for full programmes. Afamelanotide won FDA approval as Scenesse, under application number 210797, with a maker, a label and studies behind it. KPV is the opposite case. It is not a new version. It is the natural end piece of the body's own hormone, and no company could protect it long enough to pay for a large final-stage study. So the animal work piles up and the human column stays empty, decade after decade.
The July 2026 advisory meeting is where that emptiness met a decision. FDA's reviewers proposed not adding KPV to the list of substances pharmacies may compound. Their reasons are worth pulling apart, because they are different kinds of reason. Two are about product quality. The substance is not well described chemically, its name does not follow chemical naming standards, and the request came with no lab certificate or data on impurities. Those could be fixed by a making standard without a single new study. The third is about evidence, and that cannot be fixed the same way. FDA could not judge whether it works, because there is nothing in people to judge. The fourth is about risk, and it follows from the third. With no human data at all, including nothing on immune reactions, the risks are unknown rather than acceptable.
The strongest argument on the other side, made at these meetings in general, is that people are buying it anyway, and a regulated supply is safer than a gray-market one. That is a fair argument about supply chains. It is not evidence that the peptide does anything, and nobody at that meeting claimed it was.
A compound shows up here only when a study on its own page names this goal and reports a result for it. Just naming it is not enough. Work in people, in animals and in the lab is counted separately and never mixed. People counts come from the study lines, and when in doubt they count low. Nothing here is advice. Nothing here tells you to take or to avoid anything.